PMID- 23160045
OWN - NLM
STAT- MEDLINE
DCOM- 20130129
LR  - 20220309
IS  - 1546-1726 (Electronic)
IS  - 1097-6256 (Print)
IS  - 1097-6256 (Linking)
VI  - 15
IP  - 12
DP  - 2012 Dec
TI  - Glucocorticoid receptors recruit the CaMKIIalpha-BDNF-CREB pathways to mediate memory 
      consolidation.
PG  - 1707-14
LID - 10.1038/nn.3266 [doi]
AB  - Emotionally important events are well remembered. Although memories of emotional 
      experiences are known to be mediated and modulated by stress hormones such as 
      glucocorticoids, little is known about the underlying molecular mechanisms. We 
      found that the hippocampal glucocorticoid receptors that are critically engaged 
      during the formation of long-term inhibitory avoidance memory in rats were 
      coupled to the activation of CaMKIIalpha, TrkB, ERK, Akt, PLCgamma and CREB, as well as a 
      to a substantial induction of Arc and synaptic GluA1. Most of these changes, 
      which are initiated by a nongenomic effect of glucocorticoid receptors, were also 
      downstream of the activation of brain-derived neurotrophic factor (BDNF). 
      Hippocampal administration of BDNF, but not of other neurotrophins, selectively 
      rescued both the amnesia and the molecular impairments produced by glucocorticoid 
      receptor inhibition. Thus, glucocorticoid receptors mediate long-term memory 
      formation by recruiting the CaMKIIalpha-BDNF-CREB-dependent neural plasticity 
      pathways.
FAU - Chen, Dillon Y
AU  - Chen DY
AD  - Department of Neuroscience and Friedman Brain Institute, Mount Sinai School of 
      Medicine, New York, New York, USA.
FAU - Bambah-Mukku, Dhananjay
AU  - Bambah-Mukku D
FAU - Pollonini, Gabriella
AU  - Pollonini G
FAU - Alberini, Cristina M
AU  - Alberini CM
LA  - eng
GR  - R01 MH065635/MH/NIMH NIH HHS/United States
GR  - R37 MH065635/MH/NIMH NIH HHS/United States
GR  - F31-MH816213/MH/NIMH NIH HHS/United States
GR  - R01-MH065635/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20121118
PL  - United States
TA  - Nat Neurosci
JT  - Nature neuroscience
JID - 9809671
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Receptors, AMPA)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - TFZ3H25BS1 (glutamate receptor ionotropic, AMPA 1)
SB  - IM
CIN - Nat Rev Neurosci. 2013 Jan;14(1):4-5. PMID: 23212549
MH  - Animals
MH  - Avoidance Learning/physiology
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*physiology
MH  - Cyclic AMP Response Element-Binding Protein/*physiology
MH  - Male
MH  - Memory, Long-Term/*physiology
MH  - Protein Transport/physiology
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, AMPA/*physiology
PMC - PMC3509234
MID - NIHMS416122
EDAT- 2012/11/20 06:00
MHDA- 2013/01/30 06:00
PMCR- 2013/06/01
CRDT- 2012/11/20 06:00
PHST- 2012/05/29 00:00 [received]
PHST- 2012/10/18 00:00 [accepted]
PHST- 2012/11/20 06:00 [entrez]
PHST- 2012/11/20 06:00 [pubmed]
PHST- 2013/01/30 06:00 [medline]
PHST- 2013/06/01 00:00 [pmc-release]
AID - nn.3266 [pii]
AID - 10.1038/nn.3266 [doi]
PST - ppublish
SO  - Nat Neurosci. 2012 Dec;15(12):1707-14. doi: 10.1038/nn.3266. Epub 2012 Nov 18.